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长链非编码RNA MALAT1与前列腺癌的关系

[Relationship between long non-coding RNA MALAT1 and prostate cancer].

作者信息

Zhang Fa, Wu Chang-Fu, Luo Yu-Hong, Zhou Feng-Hai

机构信息

Department of Urology, Lanzhou University First Hospital / The First School of Clinical Medicine, Lanzhou University, Lanzhou, Gansu 730000, China.

Department of Urology, Gansu Provincial Hospital, Lanzhou, Gansu 730000, China.

出版信息

Zhonghua Nan Ke Xue. 2020 Feb;26(2):174-179.

PMID:33346423
Abstract

Prostate cancer (PCa), as a malignant tumor originating in the prostate glandular epithelium, has become a global "killer" that threatens the health of elderly men. PCa-related studies have been focusing on the progression mechanisms and treatment strategies of the malignancy, particularly on the role of long non-coding RNA (lncRNA) in recent years. The lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) plays a key role in the progression and treatment of PCa, as well as in its metastasis and invasion and cell proliferation. lncRNA MALAT1 not only influences the biological characteristics of PCa, but also has a regulatory effect on the medicinal treatment of the disease, its action mechanisms involving ceRNA and AR signaling pathways. This review focuses on the relationship between lncRNA MALAT1 and PCa, aiming to provide a new research direction for the diagnosis and treatment of the malignancy.

摘要

前列腺癌(PCa)作为一种起源于前列腺腺上皮的恶性肿瘤,已成为威胁老年男性健康的全球性“杀手”。与PCa相关的研究一直聚焦于该恶性肿瘤的进展机制和治疗策略,尤其是近年来长链非编码RNA(lncRNA)的作用。长链非编码RNA转移相关的肺腺癌转录本1(MALAT1)在PCa的进展、治疗以及转移、侵袭和细胞增殖过程中发挥着关键作用。lncRNA MALAT1不仅影响PCa的生物学特性,还对该疾病的药物治疗具有调节作用,其作用机制涉及竞争性内源RNA(ceRNA)和雄激素受体(AR)信号通路。本综述聚焦于lncRNA MALAT1与PCa之间的关系,旨在为该恶性肿瘤的诊断和治疗提供新的研究方向。

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[Relationship between long non-coding RNA MALAT1 and prostate cancer].长链非编码RNA MALAT1与前列腺癌的关系
Zhonghua Nan Ke Xue. 2020 Feb;26(2):174-179.
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引用本文的文献

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LncRNA-MALAT1 Regulates Cancer Glucose Metabolism in Prostate Cancer via MYBL2/mTOR Axis.长链非编码 RNA-MALAT1 通过 MYBL2/mTOR 轴调控前列腺癌中的肿瘤葡萄糖代谢。
Oxid Med Cell Longev. 2022 May 2;2022:8693259. doi: 10.1155/2022/8693259. eCollection 2022.